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Child Health > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Viruses that can trigger T1DM

A

Coxsackie B virus

Enterovirus

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2
Q

Ideal blood glucose concentration

A

4.4-6.1mmol/L

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3
Q

T1DM presentation

A 
Polyuria
Polydypsia
Weight loss
Secondary enuresis
Recurrent infections 
Symptoms present 1-6weeks before developing DKA
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4
Q

Bloods for T1DM

A

FBC, UE
Blood culture if fever
HbA1c
TFT, TPO to test for autoimmune thyroid disease
Anti-TTG for coeliac disease
Insulin antibodies, anti-GAD antibodies, islet cell antibodies

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5
Q

Management of T1DM

A

Subcutaneous insulin regimes
Monitoring dietary carbohydrate intake
Monitoring blood sugar levels on waking, at each meal and before bed
Monitoring for and managing complications, both short and long term

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6
Q

Insulin in T1DM

A

Background, long acting insulin given once a day
Short acting insulin given 30minutes before meals
Insulin pump
Cycle injection sites

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7
Q

Insulin pump

A

Cannula pumps insulin into body
Replaced ever 2-3 days
To qualify: >12 and difficulty controlling HbA1c

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8
Q

Advantages of insulin pump

A

Better blood sugar control
More flexibility in eating
Fewer injections

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9
Q

Disadvantages of an insulin pump

A

Learning how to use pump
Having it attached at all times
Blockages in infusion set
Small risk of infection

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10
Q

Types of insulin pumps

A

Tethered pump

Patch pump

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11
Q

Tethered pumps

A

Replaceable infusion sets and insulin
Attached to patients belt or around waist
Controls on pump

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12
Q

Patch pumps

A

Sit directly on skin without visible tubes
Entire patch has to be replaced
Controlled by separate remote

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13
Q

T1DM hypoglycaemia causes

A 
Too much insulin
Not enough carbohydrates
Not processing carbohydrates properly
Malabsorption 
Diarrhoea
Vomiting
Sepsis
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14
Q

Hypoglycaemia symptoms

A 
Tremor
Sweating
Irritability
Dizziness
Pallor

Reduced consciousness
Coma and death

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15
Q

Management of mild hypoglycaemia

A

Rapid acting glucose

Slower acting carbohydrates

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16
Q

Management of severe hypoglycaemia

A

IV 10% dextrose:
2mg/kg bolus
5mg/kg bolus

IM glucagon

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17
Q

Causes of hypoglycaemia

A 
Hypothyroidism
Glycogen storage disorders
Growth hormone deficiency
Liver cirrhosis
Alcohol and fatty oxidation defects
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18
Q

Nocturnal hypoglycaemia

A

Sweating overnight

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19
Q

Long term macrovascular complications of hyperglycaemia

A

Coronary artery disease
Peripheral Ischaemia: poor healing, ulcers, diabetic foot
Stroke
Hypertension

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20
Q

Long term microvascular complications of hyperglycaemia

A

Peripheral neuropathy
Retinopathy
Kidney disease, glomerulosclerosis

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21
Q

Infection-related complications of hyperglycaemia

A

UTI
Pneumonia
Skin and soft tissue infections, especially in the feet
Fungal infections, especially oral and vaginal candidiasis

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22
Q

T1DM monitoring

A

HbA1c every 3-6 months
Capillary blood glucose
Flash glucose monitoring: Libre, checks glucose in interstitial fluid, 5 minute lag behind blood glucose. Need replacing every 2 weeks

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23
Q

T2DM in children

A 
Increased body weight 
Increased risk of renal complications
HTN
Dyslipidaemia
Increased cardiovascular risk
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24
Q

T2DM treatment

A

Lifestyle modification
Paediatric dietician to optimise body-weight and blood glucose control
Anti diabetic drugs
>6 months influenza and pneumococcal immunisation

Target HbA1c: 48mmol.mol

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25
Q

Anti diabetic drugs in children

A

Only Metformin hydrochloride
Increase dose gradually
3-4 months

If not working, add long acting insulin or once-daily human isophane insulin

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26
Q

DKA main problems

A

Ketoacidosis
Dehydration
Potassium imbalance

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27
Q

Potassium imbalance DKA

A 
No insulin to drive potassium into cells
Serum K high, total K low 
Kidneys remove K as serum K is high
Add insulin, hypokalaemia, low serum potassium 
Arrhythmias
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28
Q

Cerebral oedema DKA

A 
Dehydration, high blood sugar
Water moves ICF-> ECF in brain 
Brain cells shrink and become dehydrated
Rapid correction of dehydration and hyperglycaemia
ECF-> ICF
Brain swells and becomes oedematous
Brain cell destruction and death
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29
Q

Signs of cerebral oedema

A

Headaches
Altered behaviour
Bradycardia
Changes to consciousness

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30
Q

Management for cerebral oedema

A

Slowing IV fluids
IV mannitol
IV hypertonic saline

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31
Q

Presentation of DKA

A 
Hyperglycaemia, dehydration, acidosis
Polyuria
Polydipsia
N/V
Weight loss
Acetone smell to breath
Dehydration and subsequent hypotension
Altered consciousness
Symptoms of underlying trigger (sepsis)
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32
Q

DKA diagnosis

A

Blood glucose >11
Ketosis >3 mmol/l
Acidosis pH<7.3

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33
Q

Principles of DKA management in children

A 
Correct dehydration over 48 hours
Fixed rate insulin infusion
Avoid fluid boluses
Treat underlying triggers
Prevent hypoglycaemia: IV dextrose once blood glucose falls <14mmol/L
Add potassium to IV fluids and monitor serum potassium closely
Monitor for signs of cerebral oedema
Monitor glucose, ketones and pH
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34
Q

Addison’s disease

A

Adrenal glands damaged
Reduced cortisol and aldosterone secretion
Primary adrenal insufficiency
Autoimmune cause

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35
Q

Secondary adrenal insufficiency

A

Inadequate ACTH stimulating adrenal glands
Low levels of cortisol released
Congenital underdevelopment of pituitary gland
Pituitary Hypoplasia, surgery, infection, loss of blood flow, radiotherapy

36
Q

Tertiary adrenal insufficiency

A

Inadequate CRH released by hypothalamus

Long term oral steroids (>3 weeks) causing suppression of hypothalamus

37
Q

Features of adrenal insufficiency in babies

A 
Lethargy 
Vomiting
Poor feeding
Hypoglycaemia
Jaundice
Failure to thrive
38
Q

Features of adrenal insufficiency in older children

A

N/V
Poor weight gain or weight loss
Reduced appetite (anorexia)
Abdominal pain
Muscle weakness or cramps
Developmental delay or poor academic performance
Bronze hyperpigmentation to skin in Addisons: high ACTH levels which stimulate melanocytes

39
Q

Adrenal insufficiency investigations

A

UE: hyponatraemia, hyperkalaemia, hypoglycaemia

Test for cortisol, ACTH, aldosterone and renin levels

40
Q

Addison’s disease hormone levels

A

Low cortisol
High ACTH
Low aldosterone
High renin

41
Q

Secondary adrenal insufficiency

A

Low cortisol
Low ACTH
Normal aldosterone
Normal renin

42
Q

Short synacthen test

ACTH stimulation test

A

Performed in morning when adrenal glands are most fresh
Test involves giving synacthen
Blood cortisol measured at baseline, 30 and 60 minutes after administration
Cortisol level should at least be double in response to synacthen

43
Q

Management of adrenal insufficiency

A

Replacement steroids
Hydrocortisone for cortisol (glucocorticoid)
Fludrocortisone for aldosterone (mineralocorticoid)
Steroid card and emergency ID tag
Increases doses in acute illness

44
Q

Monitoring of adrenal insufficiency

A 
Growth and development
Blood pressure 
U&Es
Glucose
Bone profile
VitaminD
45
Q

During acute illness (sick day rules)

A

> 38degrees temperature
Vomiting and diarrhoea
Dose of steroid increased and given more regularly
Blood sugar needs to be monitored closely
Need to eat food containing carbohydrates regularly
D/V, need IM injection of steroid at home and likely required admission for IV steroids

46
Q

Addisonian crisis

A

Acute presentation of severe Addisons
Reduced consciousness
Hypotension
Hypoglycaemia, hyponatraemia, hyperkalaemia

47
Q

Management of Addisonian crisis

A 
Intensive monitoring
Parenteral steroids 
IV fluid resuscitation
Correct hypoglycaemia
Careful monitoring of electrolytes and fluid balance
48
Q

Polydipsia in children

A

Central diabetes insipidus
Nephrogenic diabetes insipidus
Diabetes mellitus TY1
Diabetes mellitus TY2

49
Q

Puberty in males

A

First sign: testicular growth at 12 years
Testicular volume >4ml indicates onset of puberty
Maximum height spurt at 14

50
Q

Puberty in females

A

First sign is breast development at 11.5 years of age
Height spurt reaches maximum at 12, before menarche
Menarche at 13

51
Q

Normal changes in puberty

A

Gynaecomastia may develop in boys
Asymmetrical breast growth may occur in girls
Diffuse enlargement of the thyroid gland may be seen

52
Q

Delayed puberty with short stature

A

Turner’s syndrome
Prader-Willi syndrome
Noonan syndrome

53
Q

Delayed puberty with normal stature

A

Polycystic ovarian syndrome
Androgen insensitivity
Kallman’s syndrome
Klinefelter’s syndrome

54
Q

Precocious puberty

A

Development of secondary sexual characteristics before 8 years in females and 9 years in males
More common in females

Gonadotropin dependent, gonadotropin independent

55
Q

Gonadotropin dependent precocious puberty

A

Due to premature activation of HPA axis

FSH/LH raised

56
Q

Gonadotropin independent precocious puberty

A

Due to excess sex hormones

FSH/ LH low

57
Q

Testes precocious puberty

A

Bilateral enlargement= gonadotropin release from intracranial lesion
Unilateral enlargement- gonadal tumour
Small tests: adrenal cause, tumour or adrenal hyperplasia

58
Q

Organic causes of precocious puberty in females

A

Usually idiopathic or familial and follows normal sequence of puberty
Organic cases are rare
McCune Albright syndrome

59
Q

Congenital adrenal hyperplasia

A

Congenital deficiency of 21-hydroxylase enzyme
Underproduction of cortisol and aldosterone
Over production of androgens from birth
Autosomal recessive inheritance

60
Q

Testosterone function

A

Androgen hormone
High levels in men
Low levels in women
Promotes male sexual characteristics

61
Q

Glucocorticoids function

A

Deal with stress, raise blood glucose, reduce inflammation, suppress immune system
Cortisol: main glucocorticoid hormone
Level of cortisol fluctuates during the day, higher levels in morning and during times of stress
Released in response to ACTH from anterior pituitary

62
Q

Mineralocorticoid hormones

A

Act on kidneys to control balance of salt and water in blood
Aldosterone secreted by adrenals in response to renin
Acts on kidneys to increase sodium reabsorption into blood and increase potassium secretion into urine
Aldosterone acts to increase sodium and decrease potassium in the blood

63
Q

Pathophysiology congenital adrenal hyperplasia

A

21-hydroxylase Converts progesterone into aldosterone and cortisol
21-hydroxylase deficiency
Excess progesterone -> testosterone

64
Q

Presentations in severe cases of CAH

A

Virilised genitalia: ambiguous genitalia and an enlarged clitoris due to the high testosterone levels
Severe CAH: hyponatraemia, hyperkalaemia, hypoglycaemia

Poor feeding
Vomiting
Dehydration
Arrhythmias

65
Q

Female patients mild CAH

A 
Tall for their age
Facial hair
Absent periods
Deep voice
Early puberty
66
Q

Male patients with mild CAH

A 
Tall for their age
Deep voice
Large penis 
Small testicles
Early puberty
67
Q

Management of CAH

A

Cortisol replacement with hydrocortisone
Aldosterone replacement, fludrocortisone
Virilised genitals: corrective surgery

68
Q

Congenital growth hormone deficiency

A

Disruption to growth hormone axis at hypothalamus or pituitary gland
GH1 or GHRHR mutation
Empty sella syndrome: pituitary gland is underdeveloped or damaged

69
Q

Acquired growth hormone deficiency

A

Secondary to infection, trauma, surgical interventions

70
Q

Multiple pituitary hormone deficiency

A 
Hypopituitarism 
Hypothyroidism
Growth hormone deficiency
Adrenal insufficiency
Gonadotropin
71
Q

Presentation of GH deficiency in neonates

A

Micro penis
Hypoglycaemia
Severe jaundice

72
Q

Presentation of GH deficiency in older infants and children

A

Poor growth, usually stopping or severely slowing from age 2-3
Short stature
Slow development of movement and strength
Delayed puberty

73
Q

GH deficiency investigations

A

GH stimulation test: use glucagon, insulin, arginine or clonidine
Thyroid and adrenal deficiency
MRI brain for pituitary or hypothalamus abnormalities
Genetic testing for Turner, Prader-Willi
X-RAY or DEXA scan to determine bone age and help predict final height

74
Q

Treatment of GH deficiency

A

Daily s.c. Somatropin (GH)
Treatment of other associated hormone deficiencies
Close monitoring of height and development

75
Q

Congenital hypothyroidism

A

Dysgenesis or dyshormonogenesis

Newborn blood spot screening test

76
Q

Congenital hypothyroidism presentation

A 
Prolonged neonatal jaundice
Poor feeding
Constipation
Increased sleeping
Reduced activity
Slow growth and development
77
Q

Acquired hypothyroidism causes

A

Autoimmune thyroiditis (Hashimotos)
TY1DM and coeliac associations
Anti thyroid peroxidase antibodies and anti thyroglobulin antibodies

78
Q

Symptoms of acquired hypothyroidism

A 
Fatigue and low energy
Poor growth
Weight gain
Poor school performance
Constipation
Dry skin and hair loss
79
Q

Management of hypothyroidism

A

TFTs
Thyroid ultrasound
Thyroid antibodies

Levothyroxine O.D.

80
Q

Thyrotoxicosis in pregnancy

A

Increase in TBG, increase in levels of total thyroxine but doesn’t affect free thyroxine level
Untreated thyrotoxicosis increases risk of foetal loss, maternal heart failure and premature labour
Graves most common cause
HCG can activate TSH receptor: transient gestational hyperthyroidism

81
Q

Management of hyperthyroidism in pregnancy

A

First trimester: propylthiouracil
Second trimester: carbimazole

T3/4 levels checked, don’t want hypothyroidism in fetus
TSH-receptor simulating antibodies check at 30-36 weeks

82
Q

What BMI centile would you consider tailored clinical intervention for obesity?

A

> 91st

83
Q

When BMI centile would you consider assessing for obesity comorbidities?

A

> 98th centile

84
Q

Risk factors for obesity in children

A

Asian children
Female children
Taller children: >50th percentile in height

85
Q

Cause of obesity in children

A 
GH deficiency 
Hypothyroidism
Down’s syndrome
Cushing’s syndrome
Prader-Willi syndrome
86
Q

Consequences of obesity in children

A

Orthopaedic problems: SUFE, Blount’s disease, MSK pains
Psychological consequences: poor self-esteem, bullying sleep apnoea
Benign intracranial HTN
TY2DM
HTN
Ischaemic heart disease

Child Health (20 decks)

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